Annexin A5 in cardiovascular disease and systemic lupus erythematosus

Cederholm, Anna; Frostegård, Johan

doi:10.1016/j.imbio.2005.10.007

Cited by 34 publications

(20 citation statements)

References 74 publications

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“…They are involved in a number of intra-and extracellular processes such as signal transduction, differentiation, membrane trafficking, and organization (17,34). Although the physiological function of annexins is as yet poorly understood, a growing body of evidence suggests that dysregulation in their expression and/or localization can play a role in numerous diseases leading to the term of "annexinopathies" (7,8,17,21,32).…”

mentioning

confidence: 99%

Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Monceau¹,

Belikova²,

Kratassiouk³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Monceau, Virginie, Yulia Belikova, Gueorgui Kratassiouk, Estelle Robidel, Françoise Russo-Marie, and Daniele Charlemagne. Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone. Am J Physiol Heart Circ Physiol 291: H965-H971, 2006. First published February 24, 2006 doi:10.1152/ajpheart.01053.2005.-Annexin A5 is a Ca 2ϩ -dependent phospholipid binding protein well known for its high phosphatidylserine affinity. In vitro, translocation to sarcolemma and externalization of endogenous annexin A5 in the cardiomyocyte has recently been demonstrated to exert a proapoptotic effect. To determine whether these in vitro findings occurred in vivo, we performed myocardial infarction (MI) and studied the time course of apoptosis and annexin A5 localization (0.5 to 8 h) in the border zone around the infarcted area. This zone that was defined as Evans blue unstained and triphenyltetrazolium chloride (TTC) stained, represented 42.3 Ϯ 5.5% of the area at risk and showed apoptotic characteristics (significant increases in caspase 3 activity 2.3-fold at 0.5 h; P Ͻ 0.05), transferase-mediated dUTP nick-end labelingpositive cardiomyocytes (15.8 Ϯ 0.8% at 8 h), and DNA ladder. When compared with sham-operated rats, we found that in this area, annexin A5 was translocated to the sarcolemma as early as 0.5 h after MI and that translocation increased with time. Moreover, the amount of annexin A5 was unchanged in the border zone and decreased in the infarcted area after 1 h (77.1 Ϯ 4.8%; P Ͻ 0.01 vs. perfused area), suggesting a release in the latter but not in the former. In conclusion, we demonstrated that annexin A5 translocation is an early and rapid event of the whole border zone, likely due to Ca 2ϩ increase. Part of this translocation occurred in areas where apoptosis was later detected and suggests that in vivo as in vitro annexin A5 might be involved in the regulation of early apoptotic events during cardiac pathological situations. myocardial ischemia; terminal deoxyribonucleotide transferase ANNEXINS are a structurally related family of proteins known to bind phospholipids in a Ca 2ϩ

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mentioning

confidence: 99%

Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Monceau¹,

Belikova²,

Kratassiouk³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…As an anticoagulant protein, ANX A5 also inhibits activated thrombocytes aggregation or their fusion with tissue factor-bearing microvesicles [3]. Our total SLE group showed a weak positive correlation between plasma ANX A5 and thrombocyte count per unit blood volume.…”

Section: Discussionmentioning

confidence: 57%

“…It has also been found that ischemia might cause ANX A5 concentrations increase [3]. However, attempts to determine ANX A5 levels in plasma of patients with atherosclerotic disease did not give convincing results; lower plasma concentrations were found in the acute stage of myocardial infarction [22].…”

Section: Discussionmentioning

confidence: 99%

“…Due to structural similarities, twelve of over a thousand proteins of the annexin superfamily have been classified in the annexin A family [1][2][3][4]. Under physiological conditions, annexins are involved in cell signaling, membrane trafficking events, the process of blood coagulation, and inflammation [1,2,[5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…Under physiological conditions, annexins are involved in cell signaling, membrane trafficking events, the process of blood coagulation, and inflammation [1,2,[5][6][7][8]. The best known is annexin A5 (ANX A5-previously also referred to as placental anticoagulant protein I, vascular anticoagulant a, calphobindin I) [3]. It has been found intracellularly in cellular vesicles and plasma membranes.…”

Section: Introductionmentioning

confidence: 99%

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Annexin A5 and anti-annexin antibodies in patients with systemic lupus erythematosus

Hrycek

Cieślik

2011

Rheumatol Int

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Plasma levels of annexin A5 (ANX A5) and anti-annexin A5 (aANX A5) antibodies were evaluated in 51 women with systemic lupus erythematosus (SLE). The results were compared between the total SLE group, subgroups on/without immunosuppressive therapy and the control (28 women). The relationships between ANX A5/aANX A5 antibodies levels and laboratory variables (anti-cardiolipin antibodies-aCL, total cholesterol, thrombocyte count, activated partial thromboplastin time-APTT, prothrombin time, international normalized ratio-INR) were performed in the total SLE group and in the patient subgroups identified as the arithmetic mean of ANX A5 concentration in the control plus 1-4 standard deviations (SD). The whole SLE group and the subgroup on immunosuppression showed significantly higher ANX A5 and IgG aANX A5 antibodies concentrations. A weak positive correlation was found between ANX A5 and thrombocyte count, a moderate one between IgG and IgM aANX A5 antibodies, a weak negative correlation between IgG aANX A5 and APTT in the whole SLE group. SLE subgroups with ANX A5 concentrations higher than the control mean plus 3 or 4 SD showed a weak/moderate negative correlation of this parameter with aANX A5 antibodies, moderate one with IgG aCL antibodies levels, a moderate positive correlation with cholesterol concentration, moderate/high positive correlations with thrombocyte count. The association between plasma ANX A5/IgG aANX A5 levels and severity of disease was noticed. The role of aANX A5 and IgG aCL antibodies as causative factors of increased ANX A5 levels was suggested, and the relationship between ANX A5 and thrombocyte count was revealed.

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Premature atherosclerotic cardiovascular disease in systemic lupus erythematosus

Westerweel¹,

Luyten²,

Koomans³

et al. 2007

Arthritis & Rheumatism

113

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Annexin A5 in cardiovascular disease and systemic lupus erythematosus

Cited by 34 publications

References 74 publications

Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Annexin A5 and anti-annexin antibodies in patients with systemic lupus erythematosus

Premature atherosclerotic cardiovascular disease in systemic lupus erythematosus

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